Example Of Epigenetic Synthesis
Epigenetics is the series of chemical modifications of DNA and its connected proteins that contain phenotypic information during cell division. These modifications alter gene expression without changing DNA sequence. They differ among tissues and change over throughout the organism’s lifetime. A well-understood example of epigenetic modification is DNA methylation, the process by which a methyl group is covalently bonded to cytosine. During DNA replication, a specific enzyme recognizes unmethylated daughter CpGs and adds methyl groups to them. Chromatin modification, which can occur structurally or chemically, is another example of epigenetic activity.
As stated above, epigenetic modifications control gene expression. Specifically, DNA methylation
is known to inhibit gene expression. Hundreds of chromatin modifications are also known to either activate or silence genes. For example, proteins and transcription factors work together to acetylate or deacytlate histones in order to respectively activate or silence genes. This silencing and activation of genes is central to differentiation of tissues in the body as well as to the organism’s health.
Cancer is one of the most important examples of epigenetic disease in humans. In 1983, hypomethylation was discovered in colorectal cancer. Since then, DNA hypomethylation in cancer has been proven to cause unusual gene activation, chromosomal reconfiguration, and genetic instability. Hypermethylation also plays a prominent role in cancer as excess methyl groups are added to gene promoters in tumor suppressor genes. As a result of hypomethylation and hypermethylation in cancer, genes that should be off are activated, whereas genes that should be on are inhibited.
Epigenetic factors can even cause single gene disorders that adversely affect gene expression. In Rett Syndrome, for example, developmental progress is lost over time. The culprit is atypical gene expression within the brain, caused by a deficit in a protein that recognizes methylated DNA and aids in reducing gene expression. Cells that are affected by single gene disorders can have anomalies in expressing genes that are related to development, immunity, and neurological function. In any case, epigenetic diseases alter the normal ability to adapt one’s phenotype in response to environmental changes.
Aging, or the gradual reduction of phenotypic plasticity, may be closely related to many epigenetic human diseases. As phenotypic plasticity is lost, the effects of disease associated with genetic variation are intensified. If aging is related to epigenetic disease, then differences in epigenetic marks should be easily observable and measurable throughout one’s lifetime. Epigenetics of diseases are being studied more extensively in recent years. It is quite possible that new therapies can be used to treat epigenetic diseases, because epigenetic alterations are reversible. One method of therapy utilizes agents that modify the entire genome. The disadvantage to these global drugs is that they can affect genes that do not need to be treated. Another therapy method is to administer medicine that repairs biochemical pathways that were changed by epigenetic disease. It may even be possible to prevent adverse environmental effects on the genome, to mitigate the effects of destructive genes, and direct environmental influences on phenotypic plasticity.
As stated above, epigenetic modifications control gene expression. Specifically, DNA methylation
is known to inhibit gene expression. Hundreds of chromatin modifications are also known to either activate or silence genes. For example, proteins and transcription factors work together to acetylate or deacytlate histones in order to respectively activate or silence genes. This silencing and activation of genes is central to differentiation of tissues in the body as well as to the organism’s health.
Cancer is one of the most important examples of epigenetic disease in humans. In 1983, hypomethylation was discovered in colorectal cancer. Since then, DNA hypomethylation in cancer has been proven to cause unusual gene activation, chromosomal reconfiguration, and genetic instability. Hypermethylation also plays a prominent role in cancer as excess methyl groups are added to gene promoters in tumor suppressor genes. As a result of hypomethylation and hypermethylation in cancer, genes that should be off are activated, whereas genes that should be on are inhibited.
Epigenetic factors can even cause single gene disorders that adversely affect gene expression. In Rett Syndrome, for example, developmental progress is lost over time. The culprit is atypical gene expression within the brain, caused by a deficit in a protein that recognizes methylated DNA and aids in reducing gene expression. Cells that are affected by single gene disorders can have anomalies in expressing genes that are related to development, immunity, and neurological function. In any case, epigenetic diseases alter the normal ability to adapt one’s phenotype in response to environmental changes.
Aging, or the gradual reduction of phenotypic plasticity, may be closely related to many epigenetic human diseases. As phenotypic plasticity is lost, the effects of disease associated with genetic variation are intensified. If aging is related to epigenetic disease, then differences in epigenetic marks should be easily observable and measurable throughout one’s lifetime. Epigenetics of diseases are being studied more extensively in recent years. It is quite possible that new therapies can be used to treat epigenetic diseases, because epigenetic alterations are reversible. One method of therapy utilizes agents that modify the entire genome. The disadvantage to these global drugs is that they can affect genes that do not need to be treated. Another therapy method is to administer medicine that repairs biochemical pathways that were changed by epigenetic disease. It may even be possible to prevent adverse environmental effects on the genome, to mitigate the effects of destructive genes, and direct environmental influences on phenotypic plasticity.